Metabolism
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Two diabetic patients in coma
Key points from this exercise:
Both hypoglycaemia and hyperglycaemia can lead to coma:
hypoglycaemia leads to coma as a result of impairment of energy-yielding metabolism in the brain
hyperglycaemia leads to coma as a result of increased osmolality of body fluids (both directly and as a result of the diuresis caused by excretion of glucose in the urine).
Excessive administration of insulin (or excessive secretion by an insulin-secreting tumour, an insulinoma) leads to profound hypoglycaemia; plasma non-esterified fatty acid and ketone body concentrations are abnormally low because both lipolysis in adipose tissue and ketogenesis in the liver are down-regulated in response to insulin.
Failure to inject insulin in people with type I diabetes leads to hyperglycaemia with very elevated plasma concentrations of non-esterified fatty acids and ketone bodies. This is the result of the actions of glucagon, unopposed by insulin. Glucagon stimulates glycogenolysis and gluconeogenesis in the liver, so contributing to the hyperglycaemia. In the absence of insulin, hormone-sensitive lipase in adipose issue is active, leading to release of non-esterified fatty acids; glucagon stimulates ketogenesis in the liver.
Hyperglycaemia with ketoacidosis is rare in people with type II diabetes because they do secrete insulin to counteract the actions of glucagon, but not enough to overcome the resistance of tissues to insulin action.
Total pancreatectomy would have serious effects on the ability to digest starches, proteins and triacylglycerols, as well as causing major disruption of the control over the supply of metabolic fuels in both the fed and fasting states.